Download Thyroid disease: hyperthyroidism, hypothyroidis Diffuse toxic goiter

Thyroid disease: hyperthyroidism, hypothyroidis
Diffuse toxic goiter (DTG) - organ-specific autoimmune disease caused by an increased secretion of
thyroid hormones T4 and T3, and is characterized mainly by changes in the cardiovascular and nervous
systems. Most often occurs between the ages of 20-50 years, more often in women than in men. The
ratio of patients with male / female is 10:1.
Etiology. Predisposing moment is heredity. Found that Graves has in a number of generations in
families, identifies thyroid antibodies in the blood relatives of patients have a high incidence of other
autoimmune diseases among family members (type I diabetes. Addison's disease, pernicious anemia,
Myastenia gravis) and the presence of HLA-specific antigen (Bs. DR3). Female neuroendocrine
determines disposition of the body (pregnancy, laktannya. Menstrual cycle, menopause) and makes it
prone to the disease. Contributing factors believed adolescence and neurotic constitution, ie DAI.
Disease contributes to trauma, acute and chronic infections (flu, acne, rheumatism, tuberculosis, etc.),
traumatic brain injury, hyperthermia, pregnancy, taking large doses of iodine (iodine Basedow).
Pathogenesis. In most of the European population is associated with the development of Graves'
carriage histocompatibility complex genes HLA-B8 or DR-3 (weak association). We study the association
with the allele HLA-OQAI-0501, and the possible mutations of the genes governing the immune system:
interleukin receptor gene, the gene for the receptor of T-cells, in particular gene CTLA - 4. Currently,
Graves is considered as an autoimmune genetic disease. Suggest that it is the result of a birth defect of
immune control. Due to a defect of T-suppressor cells (a subtype of T-lymphocytes), who hold under
normal conditions "forbidden clones of T-lymphocytes, are their survival and proliferation." Forbidden
clones of T cells interact with organ-antigen of the thyroid gland. As a result of this interaction is
involved in immune B cells responsible for the production of antibodies. With the help of T-helperlymphocytes and plasma cells synthesize tireoidstimuliruyuschie immunoglobulins (antibodies) in the
class G. These immunoglobulins interact with receptors of follicular epithelium. This interaction has TSHlike effect, resulting in increased thyroid function.
In the development of clinical hyperthyroidism attach some importance to the increase in sensitivity of
adrenergic catecholamines. Clinical manifestations are due to biological (ffektom thyroid hormones and
catecholamines.
Classification. Graves' disease is divided on the degree of severity and the degree of increase of goitre
(and Nikolaev 5 degrees and 2 degrees on the cart).
There are 2 ways assess the severity of hyperthyroidism:
Option I used until recently
- Mild - heart rate of 80-100 beats per g, no atrial fibrillation, sudden weight loss, reduced performance
slightly, a faint tremor of the hands.
- Average degree - heart rate from 100-120 beats per minute., Increased pulse pressure, no atrial
fibrillation, a weight loss of up to 10 kg, reduced performance;
- Severe - heart rate of 120 beats per minute or more, atrial fibrillation, thyrotoxic psychosis,
degenerative changes in parenchymatous organs, body weight greatly reduced earning capacity lost.
Option II
- Subclinical (light flow) is established primarily on the basis of the hormonal studies with clinical erased.
In the study determined a reduced level
TSH with normal levels of thyroid hormones (T4 and T3).
- Symptomatic (moderate) a full-blown disease. With hormonal study determined a reduced or
completely suppressed TSH levels in combination with increased
levels of T 4 and T
- Complicated (Severe). Complications (atrial fibrillation, heart failure, relative adrenal insufficiency
thyrogenic degenerative changes in parenchymatous organs, psychosis, acute deficit of body weight).
Clinic. The main clinical manifestation of Graves' disease is a syndrome of hyperthyroidism, excess
thyroid hormone causes disruption of the functioning of most organs and body systems. Endocrine
ophthalmopathy not a symptom of Graves' disease, as previously thought. With DTG common
fibrocystic breast disease and gynecomastia in men. Sometimes, regardless of the severity of the disease
in some patients severe symptoms relative adrenal insufficiency (thyrogenic).
Sometimes there is atypical clinical types of hyperthyroidism. For persons living in iodine-deficient areas
Graves often manifests T3 - thyrotoxicosis, clinically manifest episodes of tachycardia or atrial fibrillation
with normal T4 levels. This variant is more common in older people. They usually do not happen goiter
goiter increases slightly, reduced appetite, there are no typical changes of the skin and eyes, and in 13%
of emotional lability, at 5.2% - depression, most cardiac lesions.
Diagnosis and differential diagnosis. With sufficient evidence of clinical diagnosis is in doubt. Help
diagnose hormonal study. For Graves' disease is characterized by reduction of elevated TSH and thyroid
hormones (T4iT3). If in doubt, we recommend a functional test with the TWG. No increase in TSH with
the introduction of the TWG confirms the diagnosis of Graves' disease. When there is a rise of TSH, T4,
and T s can be suspected of TSH-producing pituitary adenoma.
Studies have shown that 80-90% of the patients with Graves' disease is found in blood TSI (thyroxine stimulating immunoglobulins). Stopping treatment with TSI level is higher than 35% leads to a relapse.
Patients receiving tireostatisticheskuyu therapy should be determined at the beginning of TSI therapy
and to have lifted the maintenance dose of the drug. With long elevated TSI should be focused on
surgical treatment.
Radioisotope study of thyroid cancer in recent years, is used much less frequently in relation to
determine a hormone in the blood. The method is based on the ability of the thyroid gland selectively
accumulate iodine, and evaluation is performed on the absorption rate JL> I, the maximum
accumulation and decay rate of activity. In healthy subjects, maximum grip Jljl comes to the 24-72h. and
20-40% of the dose indicator. Hyperthyroidism than 40% after 24 h, hypothyroidism does not exceed
15% of the dose indicator.
Radioisotope scanning (scintigraphy) reveals the presence of partial or complete substernal goiter,
presence of nodes with the differential diagnosis of Graves' disease and the functional autonomy of the
thyroid gland. Scanning is a 24h. after receiving 1.5 mCi Jljl or 2-3 mCi Ts99. '"Graves is characteristic for
magnification of the thyroid gland with increased capture of the isotope.
Ultrasound - characterized by a diffuse decrease in echogenicity and is determined by the volume of the
thyroid gland. Thyroid volume> 45 ml (CMJ) is an indication for surgical treatment.
Have to differentiate with NDCs, with rheumatic diseases (myocarditis, heart disease), tuberculosis. The
diagnosis is confirmed by increasing the content of thyroid hormone, increased absorption Jljl,
enlargement of the thyroid gland.
In severe cases it is necessary to differentiate with organic lesions of the liver, kidneys, cardiovascular
system, myastema gravis.
Well differentiated with Hashimoto goiter, subacute thyroiditis and toxic adenoma.
Treatment. The main treatments for Graves' disease consists of:
- Conservative treatment of antithyroid drugs
- Surgical treatment with the previous preparation thyrostatics
- Radioactive iodine therapy.
In various countries, dominated by different treatments. For example, in Europe, preferred conservative
treatment, as has a light iodine deficiency increases sensitivity to thyreostatics. In the U.S., where iodine
intake is high, the predominant treatment with radioactive iodine. In our country, patients generally
receive treatment thyrostatics mainly merkaptoimidazolom (merkazolil, ptamazol, carbimazole), rarely
propiltiouratsilom (propitsil). They inhibit the organification of iodine and iodotyrosines condensation,
leading to the blockade of the synthesis of thyroid hormones. Also affect the immune parameters in
particular on cellular immunity. Propylthiouracil also affects the peripheral conversion of T4 to GT3 the
treatment with these drugs euthyroid state is achieved in 50-75% of cases. Indication for these drugs are
DTG at any severity, regardless of age. It is now widely used in practice merkazolil. The optimal daily
dose in mild 15-20 mg / day., Average 20-30 mg / day., Heavy - 30-40 mg / day. and more. With the
elimination of the main manifestations of Graves' disease, achieve eutireodnogo the dose gradually
diminish. The criteria for dose reduction is the heart rate and weight of the patient. Maintenance doses
(15-15 mg / day and 2.5-10 mg'sut. Within 6-12 months to 1.5 years). Or the move to "block and
replaces" (use of high doses of opyusigelno thyreostatics with thyroxine to achieve a state of
euthyroidism) provides 40-50% of long-term remission.
Along with thyrostatics used p-blockers (atenolol-50-100 mg / day., Inderal - 80-120 mg / day.) That
cropped tachycardia and autonomic symptoms, also activate the conversion of T4 to GT3. Phenobarbital
and its products (corvalol, valokordin) may reduce gipertiroksinemiyu, increasing TSH. After about 2-4
weeks of p-blockers are slowly lifted. By this time, the patient's condition stabilizes. By 3-4 weeks in a
state of moderate euthyroidism (normal levels of thyroid hormones). Since then reduced to a
maintenance dose merkazolila parallel assigning L-thyroxine dose of 50-75 mg / day, which warns
zobogenny merkazolila effect. Treatment maintenance doses merkazolilom and L-thyroxine continues
1.5-2 years, after which drugs should be discontinued and the patient is kept under observation as
possible recurrent disease.
The most threatening complication during treatment merkazolilom (tiamazol) is agranulocytosis. Usually
for the purpose of early detection of trends leykotsitopeniya recommended in the first 3 months of
treatment to control the number of leukocytes and leukocyte blood count 1 every 7-10 days, in the
latest every 3-4 weeks.
Glucocorticoids for Graves' disease is indicated only in the development of thyrogenic adrenal
insufficiency, as well as reactions to leukopenic thyreostatics.
Surgical treatment is indicated for
- Large goiter
- Intolerance thyreostatics
- Relapse after conservative therapy
- Retrosternal goiter
- The presence of a node in the interior of cancer.
The operation is performed according to the method O.V.Nikolaeva, ie subfascial, subtotal resection of
the thyroid gland and left 5.8 g. cancer, and in relapsed 2.3 g.
High performers and safe treatment for Graves' disease is treatment with radioactive iodine-131.
Radioactive iodine is administered at a total dose of 10-15 mCi. Half-life of JL) I - 8 days.
Indications for treatment of J13 ':
- After 40 years
- Severe heart failure is contraindicated for surgical treatment
- Graves' disease and tuberculosis
- DTG and GB (severe)
- Myocardial infarction
- Neuropsychiatric disorders
- Refusal of surgery.
Contraindications:
- Pregnancy
- Lactation
- Child, youth and young age
- Big or retrosternal goiter
- Diseases of the blood, kidney, and stomach ulcer.
Complete remission after treatment occurs in 90-95% of cases. Relapse is possible in 2-5% of cases,
more often in patients with mixed goiter, and when. DTG no more than 1% of patients. Before
treatment, the radioactive J1'1 Punctures pretreatment thyrostatics, p-blockers, depending on the
severity of hyperthyroidism. Before the introduction of the radioactive treatment Jljl thyrostatics stops
for 5-7 days. After therapy J1'1 necessarily thyrostatics also continuing treatment for 2-4 weeks.
Hypothyroidism
Hypothyroidism - a clinical syndrome caused by prolonged, persistent lack of thyroid hormone in the
body, or a reduction in their biological effect at the tissue level. Overt hypothyroidism in the general
population occur in 0.2-1% of cases, the first subclinical hypothyroidism - in 7-10% of women and 2.3%
among men.
Etiology and pathogenesis. The causes of congenital hypothyroidism is:
- Aplasia and dysplasia of the thyroid gland
- Endemic goiter, congenital deficiency of TSH
- A syndrome of peripheral resistance to thyroid hormone.
In most cases, the primary hypothyroidism, which develops in the outcome:
- Autoimmune thyroiditis
- Resection of the thyroid gland
- Therapy Jl3l
- Subacute thyroiditis fibrous or specific tireoditov.
- Iatrogenic hypothyroidism (treatment thyrostatics DTG)
- Idiopathic hypothyroidism.
The pathogenesis of hypothyroidism is reduced oxidation processes, ie reduced number of enzymes
(cell) due to a deficiency of thyroid hormones. The metabolism of glycosaminoglycans leads to
infiltration of the mucous membranes, skin, subcutaneous fat, muscle, myocardium. Disruption of
water-salt metabolism compounded effect of excess vasopressin and lack of atrial natriuretic factor.
Clinic. The clinical manifestations are very diverse. Must be carefully targeted questioning of patients to
identify complaints related to hypothyroidism.
Patients concerned about the gradual weight gain, dry, thickened skin, skin discoloration (waxy, peach,
yellow), coarsening of facial features, enlargement of the shoe, blurred speech. Periodically, there are
pains in the right upper quadrant, constipation, chest pain, shortness of breath when walking. Women
often disrupted menstrual function, and the spectrum of disorders ranging from polimenorei and
mepometrorragii to amenorrhea. Reduced intelligence, they are difficult to analyze the events and
progressively reduced memory. There are roughly the following syndromes in hypothyroidism.
'Hypothermic - exchange syndrome: obesity, lowering g °-ratela.
Hypothyroid dermopathy: miksedematozy edema and periorbital edema, puffy face, big lips, tongue
with teeth prints on the edges, yellow skin (giperkarotinemiey), hearing loss, hoarse voice.
Syndrome of central and peripheral nervous system: drowsiness, confusion, memory loss, bradycardia,
muscle pain, paresthesia, decreased tendon reflexes. 'Syndrome lesions of the cardiovascular system:
the heart miksedematoznoe (bradycardia, low voltage, (T waves in the ECG, the lack of blood supply).
Lowered blood pressure, polyserositis, atypical variants (sgppertenziey. with tachycardia in NC.)
Syndrome, gastrointestinal lesions: hepatomegaly, biliary dyskinesia, colon, constipation, loss of
appetite, nausea, vomiting.
Anemic syndrome: normochromic, normocytic, hypochromic iron macrocytic, B | 2 deficiency anemia
'Syndrome giperprolaktinemicheskogo hypogonadism. TRH overproduction not only increases the
release of TSH and prolactin, which helps to reduce LH (lyuliberina), ie develops clinical syndrome Van
Wick-Hennes Rosa, manifested amenorrhea, galactorrhea, secondary polycystic ovaries.
Ectodermal syndrome disorders: hair dull, brittle, falling on his head, eyebrows, legs, slowly growing.
Syndrome "empty sella": long pituitary stimulation due to low levels of thyroid hormone leads to
pituitary adenoma. Against the background of preparations of thyroid replacement therapy decreases
the size of the sella and develops "empty sella syndrome"
Sleep apnea syndrome - develops due miksedematoznoy infiltration of the mucous membranes and
sensory disturbances of the respiratory center.
Despite the rather vivid clinical picture often misdiagnosed disease "mask" of primary hypothyroidism.
In secondary hypothyroidism usually have symptoms of deficiency of other pituitary tropic hormones.
Peculiarities of secondary hypothyroidism
1) exchange - hypothermic moment occurs without obesity, even mentioned exhaustion;
2) dermopathy is not expressed strongly, no rough swelling, skin is thinner, paler and more wrinkled:
3) there is no heart failure, hypothyroid poliserozita, hepatomegaly, B, 2 deficiency
anemia.
The most difficult and quite rare complication of hypothyroidism are: hypothyroid coma usually occurs
more frequently in older people with long-undiagnosed hypothyroidism, severe concomitant diseases
for lack of care, often in cold regions.
Provoke - cooling, treatment with barbiturates, antipsychotics, intercurrent disease. At the core genesis
is oppression of tissue respiration and function of the adrenal cortex due to prolonged hypothyroidism,
renal hypoperfusion and the syndrome of inadequate production of vasopressin (thyroid hormone and
vasopressin antagonist is).
Clinically manifest - hypothermia, hypoventilation with hyper-drip, hypervolemia. ppyunatriemiey,
bradycardia, decreased blood pressure, urinary retention (acute), dynamic ileus, hypoglycemia, heart
failure, progressive CNS inhibition (stupor, coma). Mortality rate is 80%.
Diagnostics. With hormonal study for subclinical hypothyroidism, characterized by high levels of TSH and
normal levels of T4.
Symptomatic - high TSH and low T4.
In secondary hypothyroidism - TSH and T4snizheny.
Screening for congenital hypothyroidism and researching plasma TSH levels no earlier than 4 to 5 days
after birth.
With normal or reduced TSH to TRH test performed for the differential diagnosis of primary from
secondary hypothyroidism.
Investigated baseline TSH and 30 minutes after intravenous administration 200 mg TRH in primary
hypothyroidism TSH increased to 25 mIU / L or more, a secondary level of TSH is not changed.
Classification of hypothyroidism with the pathogenesis:
a. primary (thyrogenic)
b. secondary (pituitary)
a. tertiary (hypothalamic)
g tissue (transport, peripheral)
Classification according to the gravity
and the latent (subclinical): elevated TSH with normal T4
b. symptomatic: TSH hypersecretion with reduced T4, clinical manifestations:
- Compensated
- Subcompensated
in Severe (complicated): severe complications, such as cretinism, heart failure, serous cavity effusion,
secondary pituitary adenoma
Treatment. In all forms of replacement therapy shows L-thyroxine. Treatment begins with a small dose:
the elderly 12.5 mg / day, in the presence of cardiac disease with 6.25 mg / day. Morning 30 minutes
before eating. The dose is gradually increased to a maintenance: young for 3-4 weeks, the elderly - 2-3
months., With concomitant cardiac disease - 4-6 months. Full maintenance dose of L-thyroxine is
determined by the rate of 1.6 mg / kg (for women near YuOmkg / day for men 150 mg / day) for severe
comorbidity 0.9 mg / kg, with significant obesity, the calculation is 1 kg " ideal body weight. "
Babies need 10-15 mg / kg body weight of children and 2 mg / kg. During pregnancy, the need increases
to 45%, while the level of T4 and TSH should be monitored at least 1 time in 2 months when combined
with adrenal insufficiency (Schmidt syndrome), treatment should begin with glucocorticoids and to
achieve compensation added L-thyroxine.
If the TSH level is not returned to normal after 4 months, then increase the dose for 25 mg. After
normalization of TSH control studies conducted 1 time in 6 months, then 1 per year. With age, the need
for thyroid hormone is reduced.
References:
1. Balabolkin MI Endocrinology, Moscow, 1998
2. Vladimir Potemkin Endocrinology, Moscow, 1999.
3. Grandparents II Endocrinology, Moscow, 2000.
4. G.A.Melnichenko, O.V.Udovichenko, A.E.Shvedova. Endocrinology. Typical errors practitioner-2012.
frequent errors in diagnosis and treatment of diseases of the endocrine system. Separate chapters are
devoted to diseases of pituitary, thyroid, parathyroid, obesity, osteoporosis, etc.
5. S.B.Shustov, Yu S. Khalimov GE Trufanov functional and topical diagnosis in endocrinology, 2010.
6. GA Melnichenko A.Yu.Tokmakova, D.E.Koloda, N.V.Lavrischeva. Endocrine disease. 2009 Guidelines
for Pediatric Endocrinology. Handbook of Clinical Pediatric Endocrinology Edited by Charles GD Brook,
Rosalind S. Brown. 2009.
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Endocrinology. 2010.
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Endocrinology. 2011.
9. Clinical Endocrinology. Edited by EA Kholodova. 2011.
10. Endocrinology. National guidelines (+ CD-ROM). 2012. National guidelines - a series of practical
guides for major medical specialties, including specific information needed for continuous medical
postgraduate obrazovaniya.god.
More:
1. Edited by EA Kholodova Handbook of Clinical Endocrinology. Minsk. Belarus, 1996.
2. Therapeutic Handbook (Washington, translated from English), 1996 (section endocrinology).
3. Edited by Starkova NT, Manual of Endocrinology, Medicine, 1996
4. Edited by H. Lavin, Endocrinology. Practice. Moscow, 1999.
5. Endocrinology. Diabetes. Fadeev PA A Reference Guide. 2009.
6. I.B.Manuhin, L.G.Tumilovich, M.A.Gevorkyan. Gynecological endocrinology in 2012. lectures on
gynecological endocrinology.
7. A.V.Kartelishev, Alexander Rumyantsev, N.S.Smirnova Actual problems of obesity in children and
adolescents. 2010.
8. AN ham. Emergency Endocrinology. 2011. diagnosis and treatment of emergency conditions
associated with endocrine diseases, outlines coma in patients with diabetes mellitus.
9. A.M.Mkrtumyan, A.A.Nelaeva. Emergency Endocrinology. 2010.
10. N. A.Petunina, L.V.Truhina. Thyroid disease. 2011.
11. G.M.Kronenberg, Sh.Melmed, K.S.Polonski, P.R.Larsen. Thyroid disease. Williams Textbook of
Endocrinology. 2010.
12. G.M.Kronenberg, Sh.Melmed, K.S.Polonski, P.R.Larsen. Diseases of the adrenal cortex and endocrine
hypertension. Williams Textbook of Endorcinology, 11th edition. 2010.
13. Treatment of diseases of the thyroid gland by traditional and non-traditional ways. 2010.
Internet sites:
1. "Internet Portal: HINARI»; 2. medscape.com; 3. Alltheweb.com; 4. Yahoo.com.
5. E-medicine.com.